Ignet

Gene Information

Gene symbol: ATP6AP2

Gene name: ATPase, H+ transporting, lysosomal accessory protein 2

HGNC ID: 18305

Synonyms: M8-9, APT6M8-9, ATP6M8-9

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	COX8A	1 hits
3	GGT1	1 hits
4	INS	1 hits
5	JUP	1 hits
6	MAPK3	1 hits
7	NR3C2	1 hits
8	PTGS2	1 hits
9	PVRL1	1 hits
10	SQSTM1	1 hits

Related Sentences

#	PMID	Sentence
1	18335185	(Pro)renin receptor-bound prorenin not only causes the generation of angiotensin II via the nonproteolytic activation of prorenin, it also activates the receptor's own intracellular signaling pathways independent of the generated angiotensin II.
2	18922597	The binding of prorenin to the (pro)renin receptor triggers two major pathways: the angiotensin II-dependent pathway as a result of the conversion of prorenin to the active form of prorenin through a conformational change, and the angiotensin II-independent, (pro)renin-receptor-dependent intracellular mitogen-activated protein kinase pathway.
3	18922597	The handle region peptide significantly inhibited the development of end-organ damage in these diabetic animals, and had a greater benefit than angiotensin-converting enzyme inhibitors in diabetic angiotensin II-type 1a-receptor-deficient mice.
4	20075844	Aliskiren inhibits intracellular angiotensin II levels without affecting (pro)renin receptor signals in human podocytes.
5	21177830	Recent data suggest that nicotinamide adenine dinucleotide phosphate oxidase-mediated oxidative injury to the proximal tubule, like that seen in the glomerulus, contributes to proteinuria in insulin-resistant states.
6	21177830	The vasodilator β-blocker nebivolol reduces nicotinamide adenine dinucleotide phosphate oxidase activity, increases bioavailable nitric oxide, and improves insulin sensitivity.
7	21177830	Compared with Zucker lean, ZO controls exhibited increased proteinuria and γ-glutamyl transpeptidase, reductions in systemic insulin sensitivity in association with increased renal renin, (pro)renin receptor, angiotensin II type 1 receptor, and mineralocorticoid receptor immunostaining, oxidative stress, and glomerular tubular structural abnormalities that were substantially improved with in vivo nebivolol treatment.
8	21177830	Nebivolol treatment also led to improvements in glomerular podocyte foot-process effacement and improvement in podocyte-specific proteins (nephrin and synaptopodin) as well as proximal tubule-specific proteins (megalin and lysosomal-associated membrane protein-2) and proximal tubule ultrastructural remodeling in the ZO kidney.
9	21737546	Podocyte COX-2 exacerbates diabetic nephropathy by increasing podocyte (pro)renin receptor expression.
10	21737546	In cultured podocytes overexpressing COX-2, high glucose induced cell injury and increased both expression of the pro(renin) receptor and activation of the renin-angiotensin system.
11	21737546	In vivo, podocyte pro(renin) receptor expression increased in diabetic COX-2-transgenic mice, and treatment with a COX-2 inhibitor abrogated the upregulation of (pro)renin receptor and reduced albuminuria, foot-process effacement, and mesangial matrix expansion.
12	21737546	In summary, these results demonstrate that increased expression of podocyte COX-2 predisposes to diabetic glomerular injury and that the (pro)renin receptor may be one mediator for this increased susceptibility to injury.
13	21737546	Podocyte COX-2 exacerbates diabetic nephropathy by increasing podocyte (pro)renin receptor expression.
14	21737546	In cultured podocytes overexpressing COX-2, high glucose induced cell injury and increased both expression of the pro(renin) receptor and activation of the renin-angiotensin system.
15	21737546	In vivo, podocyte pro(renin) receptor expression increased in diabetic COX-2-transgenic mice, and treatment with a COX-2 inhibitor abrogated the upregulation of (pro)renin receptor and reduced albuminuria, foot-process effacement, and mesangial matrix expansion.
16	21737546	In summary, these results demonstrate that increased expression of podocyte COX-2 predisposes to diabetic glomerular injury and that the (pro)renin receptor may be one mediator for this increased susceptibility to injury.
17	21737546	Podocyte COX-2 exacerbates diabetic nephropathy by increasing podocyte (pro)renin receptor expression.
18	21737546	In cultured podocytes overexpressing COX-2, high glucose induced cell injury and increased both expression of the pro(renin) receptor and activation of the renin-angiotensin system.
19	21737546	In vivo, podocyte pro(renin) receptor expression increased in diabetic COX-2-transgenic mice, and treatment with a COX-2 inhibitor abrogated the upregulation of (pro)renin receptor and reduced albuminuria, foot-process effacement, and mesangial matrix expansion.
20	21737546	In summary, these results demonstrate that increased expression of podocyte COX-2 predisposes to diabetic glomerular injury and that the (pro)renin receptor may be one mediator for this increased susceptibility to injury.
21	21737546	Podocyte COX-2 exacerbates diabetic nephropathy by increasing podocyte (pro)renin receptor expression.
22	21737546	In cultured podocytes overexpressing COX-2, high glucose induced cell injury and increased both expression of the pro(renin) receptor and activation of the renin-angiotensin system.
23	21737546	In vivo, podocyte pro(renin) receptor expression increased in diabetic COX-2-transgenic mice, and treatment with a COX-2 inhibitor abrogated the upregulation of (pro)renin receptor and reduced albuminuria, foot-process effacement, and mesangial matrix expansion.
24	21737546	In summary, these results demonstrate that increased expression of podocyte COX-2 predisposes to diabetic glomerular injury and that the (pro)renin receptor may be one mediator for this increased susceptibility to injury.
25	24533170	High glucose induces podocyte injury via enhanced (pro)renin receptor-Wnt-β-catenin-snail signaling pathway.
26	24533170	(Pro)renin receptor (PRR) expression is upregulated in diabetes.
27	24533170	We hypothesized that PRR contributes to podocyte injury via activation of Wnt-β-catenin-snail signaling pathway.
28	24533170	Compared to normal glucose, high glucose significantly decreased mRNA and protein expressions of podocin and nephrin, and increased mRNA and protein expressions of PRR, Wnt3a, β-catenin, and snail, respectively.
29	24533170	Cells treated with high glucose and PRR siRNA demonstrated significantly attenuated mRNA and protein expressions of PRR, Wnt3a, β-catenin, and snail; enhanced expressions of podocin mRNA and protein, improved expression and reorganization of F-actin, and reduced transwell albumin flux.
30	24533170	High glucose induces podocyte injury via enhanced (pro)renin receptor-Wnt-β-catenin-snail signaling pathway.
31	24533170	(Pro)renin receptor (PRR) expression is upregulated in diabetes.
32	24533170	We hypothesized that PRR contributes to podocyte injury via activation of Wnt-β-catenin-snail signaling pathway.
33	24533170	Compared to normal glucose, high glucose significantly decreased mRNA and protein expressions of podocin and nephrin, and increased mRNA and protein expressions of PRR, Wnt3a, β-catenin, and snail, respectively.
34	24533170	Cells treated with high glucose and PRR siRNA demonstrated significantly attenuated mRNA and protein expressions of PRR, Wnt3a, β-catenin, and snail; enhanced expressions of podocin mRNA and protein, improved expression and reorganization of F-actin, and reduced transwell albumin flux.
35	26081285	Previously, we reported that high glucose induced podocyte injury through upregulation of the (pro)renin receptor (PRR).
36	26081285	We hypothesized that increasing PRR reduces autophagy and increases apoptosis of mouse podocytes exposed to high glucose via activation of the PI3K/Akt/mTOR signaling pathway.
37	26081285	High glucose significantly increased mRNA and protein levels of PRR, phosphorylation of PI3K/Akt/mTOR, and p62.
38	26081285	In the absence of PRR, activation of Akt with sc-79 or mTOR with MHY-1485 increased p62 accumulation.
39	26081285	Based on these data, we conclude that high glucose decreases autophagy and increases apoptosis in mouse podocytes through the PRR/PI3K/Akt/mTOR signaling pathway.
40	28450279	Autophagy upregulates (pro)renin receptor expression via reduction of P62/SQSTM1 and activation of ERK1/2 signaling pathway in podocytes.
41	28450279	Knockout of p62 enhanced extracellular signal-regulated kinases (ERK1/2) activity.
42	28450279	(pro)renin receptor (PRR) is expressed in podocytes where it contributes to the homeostasis of these cells.
43	28450279	We hypothesized that in podocytes, upregulation of autophagic activity increases PRR expression via reduction of p62 and stimulation of ERK1/2 signaling pathway.
44	28450279	Both rapamycin and EBSS significantly decreased p62 protein levels, increased ERK1/2 activation by phosphorylating pTpY185/187, and increased mRNA and protein expressions of PRR.
45	28450279	Utilizing confocal microscopy demonstrated that rapamycin and EBSS significantly decreased p62/SQSTM1 and increased PRR protein expressions.
46	28450279	Similarly, by enhancing autophagic activity by transfection with autophagy-related 5 (ATG5) cDNA or ATG7 cDNA, results similar to those observed with rapamycin and EBSS treatments were produced.
47	28450279	ERK1/2 inhibitor U0126 significantly attenuated mRNA and protein expressions of PRR in podocytes treated with rapamycin.
48	28450279	In conclusion, upregulation of autophagy enhanced PRR expression through reduction of p62 and stimulation of ERK1/2 activity signaling pathway.
49	28450279	Autophagy upregulates (pro)renin receptor expression via reduction of P62/SQSTM1 and activation of ERK1/2 signaling pathway in podocytes.
50	28450279	Knockout of p62 enhanced extracellular signal-regulated kinases (ERK1/2) activity.
51	28450279	(pro)renin receptor (PRR) is expressed in podocytes where it contributes to the homeostasis of these cells.
52	28450279	We hypothesized that in podocytes, upregulation of autophagic activity increases PRR expression via reduction of p62 and stimulation of ERK1/2 signaling pathway.
53	28450279	Both rapamycin and EBSS significantly decreased p62 protein levels, increased ERK1/2 activation by phosphorylating pTpY185/187, and increased mRNA and protein expressions of PRR.
54	28450279	Utilizing confocal microscopy demonstrated that rapamycin and EBSS significantly decreased p62/SQSTM1 and increased PRR protein expressions.
55	28450279	Similarly, by enhancing autophagic activity by transfection with autophagy-related 5 (ATG5) cDNA or ATG7 cDNA, results similar to those observed with rapamycin and EBSS treatments were produced.
56	28450279	ERK1/2 inhibitor U0126 significantly attenuated mRNA and protein expressions of PRR in podocytes treated with rapamycin.
57	28450279	In conclusion, upregulation of autophagy enhanced PRR expression through reduction of p62 and stimulation of ERK1/2 activity signaling pathway.